Etiology
Pathophysiology
Seborrheic keratosis results from benign clonal expansion of epidermal keratinocytes.[15] Studies have shown an association between expression of p16 (a marker for cellular senescence) and increased number of seborrheic keratoses.[16][17][11]
Amyloid precursor protein (also a marker of cellular senescence) expression is higher in UV-exposed than in non-exposed skin and increases with age. The expression of amyloid precursor protein (APP) has been evaluated in seborrheic keratosis versus normal skin by immunohistochemistry, Western blotting, and quantitative PCR. APP and its downstream products were more strongly expressed in seborrheic keratoses than in normal skin suggesting that overexpression of APP may promote the onset of seborrheic keratoses and is a marker of skin aging and UV damage.[18]
Activating somatic fibroblast growth factor 3 (FGFR3) mutations in the epidermis have been shown to be involved in the development of seborrheic keratosis. FGFR3 mutations are already present in flat seborrheic keratosis. FGFR3 mutations are associated with increased age, and localization of lesions on the head and neck suggests a causative role of cumulative lifetime UV exposure.[13][14] There is little evidence for the hypothesis that seborrheic keratosis is due to human papillomavirus.[19]
Classification
Histologic patterns
Five distinct histologic patterns of seborrheic keratosis can be differentiated, although the different types have no clinical significance.[3][4]
Acanthotic (solid): sheets of basaloid cells with embedded horn cysts.
Reticulated (adenoid): this type shows interlacing thin strands of pigmented basaloid cells enclosing horn cysts. This variant often evolves from a solar lentigo and therefore is frequently found on the face or other chronically sun-exposed areas. This type is the only variant related to solar lentigines.
Hyperkeratosis (papillomatous): this type shows an exophytic growth with hyperkeratosis, papillomatosis, and acanthosis.
Clonal: irregular acanthosis and papillomatosis with orthokeratoses. Multiple nests of heavily pigmented basaloid cells within the epidermis.
Irritated: a heavy lichenoid inflammatory infiltrate is present in the upper dermis.
Solar lentigo
Solar lentigines (actinic lentigo, senile lentigo or "age spot") do not represent a special entity of seborrheic keratosis. They represent the initial phase of seborrheic keratosis on areas of the skin that have been heavily exposed to sunlight over decades. Therefore, they are found especially on the face and on the back of the hands. They appear as light-to-dark-brown pigmented macules with sharp borders. Over the course of years, solar lentigines become slightly elevated and darker and a distinction between seborrheic keratosis and solar lentigo is difficult to make. Histologically these lesions correspond to seborrheic keratosis with reticulated features. The number of melanocytes may be increased and the upper dermis shows solar elastosis as a consequence of the chronic UV damage. Solar lentigines/seborrheic keratosis on sun-damaged skin can undergo regression. Clinically the lesions develop a brown-grayish-blue granular appearance. Histologically this regression is explained by a band-like (lichenoid) infiltrate of lymphocytes, and therefore these lesions are referred as "lichen planus-like keratoses".
Stucco keratosis
Stucco keratoses are usually multiple, white or skin-colored, dry, well-circumscribed scaly papules often seen on the extremities (especially on lower legs and back of the hands) of older people. Stucco keratoses are associated with chronic UV damage of the skin. Histologically they cannot be differentiated from hyperkeratotic seborrheic keratosis.
Dermatosis papulosa nigra
This type of seborrheic keratosis consists of multiple small (1 to 2 mm in diameter), dark brown or black soft papules usually found on the face, neck, and chest. It is more common in people with brown and black skin (Fitzpatrick skin type IV, V, or VI) and women.
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